This laboratory has a long standing interest in mechanisms of acute inflammatory edema. Investigations by this group and others have identified important roles for PMN derived oxidants, proteases and cationic proteins in mediating acute inflammatory edema. In this proposal the investigators will extend prior observations about the edemagenic activity of fatty acids oxidized by PMN through an aspirin sensitive pathway. The specific questions that will be asked are: 1. What are the oxymetabolites of linoleic acid exposed to human PMN separated from blood? Which of the metabolites' production is inhibited by aspirin? What is the role of platelets in production of the metabolites? 2. Do stimulated PMN metabolize endothelial cell linoleate to the same oxymetabolites? 3. Do the aspirin sensitive PMN-oxymetabolites of linoleic acid increase the permeability of endothelial and epithelial cell monolayers in vitro, are they cytolytic to endothelial and epithelial cells, and do they initiate phospholipid hydrolysis in endothelial and epithelial cells? 4. What are the effects of the PMN-oxymetabolites of linoleic acid on endothelial and epithelial cell membrane ionic conductances? 5. In what PMN cellular fraction is the aspirin sensitive oxidase and is it distinct from cyclooxygenase?